Renal Flashcards

1
Q

Kidney function

A

homeostasis of internal environment
maintenance of fluid and electrolyte balance
secretion of EPO, renin, dihydroxy Vit D

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2
Q

Renal Capsule

A

tightly adhering capsule covers outer surace

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3
Q

renal cortex

A

major components include the glomeruli and portion of tubules

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4
Q

renal medulla

A

proximal/distal tubules
collecting ducts
renal pyramids

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5
Q

calyces

A

recieve urine from the large collecting ducts, have smooth muscle that contracts to move urine into the bladder

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6
Q

Minor/major Calyx

A

apex of pyramids project into a cup-shaped cavity, join together to form major calyx to join together to form the RENAL PELVIS

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7
Q

Nephron

A

selective reabsorption and secretion of ions & mechanical filtration of fluid,waste,electrolytes
regulation of acid/bases

3 types

  • superficial cortical
  • midcortical
  • juxtadullary
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8
Q

juxtaglomerular cells

A

surround the afferent artery where it enters the glomerulus

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9
Q

Juxtaglomerular apparatus

A

it controls renal blood flow, glomerular filtration, renin secretion

filtrates plasma and removes wastes but retains water/solutes

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10
Q

Parts of the nephron

A

glomerulus- production of filtrate

PCT- reabsorption of water ions and all organic nutrients

Loop of henle- further reabsorption of water (descending) and Na+ Cl- (ascending)

DCT- secretion of ions, acids, drugs, toxins, variable reabsorption of water, Na+ ions, Ca+ ions

Collecting duct- variable reabsorption of water, sodium, potassium, hydrogen bicarbonate

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11
Q

Glomerular filtration membrane

A

separates blood in the glomerular capillaries from the fluid in the bowmans space

allows all the components of blood to filter through except blood cells, plasma proteins, negatively charged proteins

releases vasodilation and vasoconstriction to regulate blood flow

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12
Q

Glomerular filtration rate

A

filtration of plasma per unit of time
degree of renal function
loss or damage to nephrons lead to decrease in GFR
normal rate 90-125 mL/min

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13
Q

renal clearance

A

vol of blood plasma cleared of a waste product in 1 minute

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14
Q

Rate of filtration depends on

A
  • pressure across different/efferent arterioles
  • pressure across glomerular capillaries
  • pressure inside bowmans capsule
  • changes in hydrostatic pressure
  • changes in diameter of arterioles
  • large molecules cannot move through small pores in glomerular membrane
  • negative charge along filtration membrane, negatively charged particles get repelled
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15
Q

Renin-angiotensin-aldosterone system (RAA)

A

ADH are the feedback loop systems maintaining homeostasis within the body

Hypothalamus releases ADH
increase in nephron permeability
additional water is absorbed
serum osmolarity normalised
ADH release stops
increase serum osmorlarity
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16
Q

Aldosterone

A

regulation of BP, acts on distal tubules & collecting duct
keeps pressure in glomerulus within a wide range of system BP

so blood flow & GFR are constant over a range of pressure 80-180

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17
Q

Renal function tests

A
  • measured by amount of renal clearance
  • amount of a substance that can be cleared from the blood by the kidneys

C= UV/P
u- rate of urine output
v- urine output
p- waste concentration in plasma

an indirect measure of GFR, tubular secretion, tubular reabsorption, renal blood flow

can measure creatine and insulin

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18
Q

creatine

A

produced by muscle
released into blood at relatively constant rate
filtered by the glomerulus
clearance overstimulates GFR

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19
Q

Anuria

A

no urine production

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20
Q

Oliguria

A

decrease urine production

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21
Q

Polyuria

A

excessive and abnormal urine production

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22
Q

Diuresis

A

increase urine production

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23
Q

Nocturia

A

urine production at night

24
Q

Haematuria

A

blood in urine

25
Azotaemia
increase blood urea, indicates renal dysfunction
26
Uraemia
above and other electrolyte/metabolic abnormalities
27
Obstructive Uropathy
Any condition,structural or functional, causing a change in the normal urine flow anywhere within urinary tract causes vary with age and gender causes pain- distention caused by blockage urine output- can vary depending on degree of blockage hypertension- (unilateral) - increase renal secretion (bilateral)-extracellular fluid vol expansion
28
partial vs complete obstruction
partial- compression and accumulation of urine, ischaemic damage and atrophy with decrease concentrating ability of the kidney complete- Decrease GFR, resulting in renal failure
29
hydroureter + hydronephrosis
hydroureter =obstruction of ureter with accumulation of urine hydronephrosis= increase in hydrostatic pressure in renal pelvis, calyces increase accumulation of urine in renal collecting system renal tubules affected first, impaired concentration, decrease GFR kidneys enlarge, pelvis/calyces dilated, calyces blunted cortical tubules lost-interstitual fibrosis\ ss pain bladder symptoms types bilateral (partial)- poluria, nocturia, acidosis, HT bilateral (complete)- oliguria, anuria unilateral - asymptomatic
30
Kidney stones patho
changes in pH and temp decrease in urinary flow high urinary concentration of stone forming substance grow in renal papilla + pelvis
31
calcium kidney stone
``` smallest hypercalciuria hyperuricosuria bone demineralisation diet high in vegetables prolonged mobility hyperparathyroidism middle aged men with a family history ```
32
struvite kidney stone
women infected by microbes | alkaline urine
33
Uric acid stone
acidic environment can cause - ulcerative colitis/ regional enteritis with fluid/ bicarbonate loss - sufferers with gout, high meat and fish diets - leukaemia
34
Cysteinuria
rare hereditary disorder disorder of amino acid metabolism decrease tubular reabsorption of cysteine SS pain, flank pain, nausea and vomiting, haematuria predisposing factors family history, diabetes, pregnancy, childhood infection, chronic disease, immunosupression, renal calculi, UT obstruction, prostate disease in older men treatment adequate analgesia, surgical removal of stones treat infection dissolve stones, prevent formation
35
Patho of Cysteinuria
high level of stone forming substance in plasma and urine high pH favours struvite and deposition of Ca2+ with oxalate, phosphates, carbonates low pH favours uric acid stones decrease urine output and high concentration found in papillae, renal tubules, calyces or pelvis, most
36
Kidney Dysfunction
1. Inadequate urine production 2. homeostasis severly impaired - fluid, electrolyte, acid-base balance - accumulation of creatinine, urea - decrease excretion of drug metabolism - inadequate reabsorption of amino acids, glucose 3. impaired conversion of Vit D - to the active form - impaired Ca2+ absorption 4. impaired secretion of erythropoietin - decrease RBC production - decrease oxygen carrying capacity of blood in bone marrow, decrease bone mineralisation
37
Glomerulonephritis (GMN)
inflammation of the glomerulus major cause of chronic kidney disease reduction 30-50% reduction of GFR- end stage renal failure primary= rapidly progressive glomerulonephritis e.g IgA neuropathy secondary= secondary to other diseases e.g diabetes, SLE, malaria, solid tumors
38
Patho of GMN
damage to glomerulus swelling, increase in permeability large protein molecules and RBC are filtered and seen in urine swelling, increase in pressure, decrease GFR causes systemic edema, HT epithelial layer of glomerular capillary membrane is disturbed change in permeability, basement membrane thickens occurs as a consequence of activation and release of a variety of mediators
39
5 types of GMN
1. Asymptomatic 2. Acute Nephritic syndrome 3. Rapidly progressive GMN 4. Nephrotic syndrome 5. Chronic Glomerulonephritis
40
Asymptomatic (IgA nephropathy)
most common form of GMN, young men, 15-30 year old -abnormal IgA binds to cells, complement stimulates inflammation & injury -40% show assymptomatic haematuria
41
Acute Nephritic syndrome
group of symptoms that occur with some disorders that cause swelling and inflammation of the glomeruli in the kidney or glomerulonephritis ss acute onset of gross haematuria, oliguria, mild-moderate proteinuria, increase creatine, HT, mild oedema, RBC/WBC in urine
42
Acute post-streptococcal glomerulonephritis (GMN)
circulating antibody- antigen complexes deposited in glomeruli complement activate inflammation WBC infiltrate & glomerular cells proliferate capillary blocked so filtration rate drops ss acute onset of fever, malaise, nausea, oliguria, haematuria, RBC in urine, mild HT, periorbital oedema treatment no specific treatment
43
Rapidly progressive GMN
- acute nephritis with glomerular damage - results in proteinuria - rapid progression to AKI with severe oliguria, anuria and irreversible kidney disease after weeks- months - 50-60 years extensive proliferation of cells into bowmans space injury is assoc by rapid decrease in glomerular function progression to renal failure, haematuria
44
Nephrotic syndrome
heavy protein loss generalised oedema characterised by pitting in the legs patho damage/ alteration to glomerular basement/membrane becomes permeable to plasma proteins decrease oncotic pressure of blood, fluid remains in tissures- edema release of inflamm mediators- thickening of walls/renal fibrosis treatment decrease salt, low fat diet, diruetics, immunosupression
45
Chronic Glomerulonephritis (CKD)
encompasses glomerular diseases with a progressive course leading to chronic kidney diseases
46
Acute Kidney Injury (AKI)
rapid/sudden deterioation of renal function resulting in retention of metabolic wastes impaired fluid/electrolyte balance ``` ss decrease urine output increase blood urea nitrogen increase serum creatinine usually reversible ```
47
Causes of AKI
prerenal- impaired blood flow, hypotension, ischaemia, decrease CO, haemorrhage, surgery intrarenal- acute glomerulonephritis or acute tubular necrosis postrenal- urinary tract obstruction
48
3 stages of AKI
``` 1. INITATION PHASE decrease perfusion, oliguria prevention of injury, lasts 1-3 weeks fluid retention/oedema, nausea/vom poor wound healing, fatigue ``` ``` 2. MAINTENANCE PHASE period of established renal injury/dysfunction may last weeks/months lowest urine output increase creatinine, BUN ``` 3.RECOVERY PHASE when injury is repaired, normal renal function re-established decrease serum creatinine, urea returning to normal function can take 3-12 months, 30% do not fully recover diruesis common
49
Chronic Kidney disease
gradual loss of nephrons until remainder cannot carry out normal renal function slow but irreversible, results in end-stage renal disease requires dialysis and maintenance for survival GFR
50
5 stages of chronic kidney disease
1. KIDNEY DAMAGE+ NORMAL GFR GFR 75% evidence of kidney damage, without GFR HT common, start to see abnormalities in composition of urine,structural changes e.g scarring ``` 2. MILD KIDNEY DAMAGE GFR 50% asymptomatic evidence of damage in urine subtle rise of plasma, creatinine, urea ``` 3. MODERATELY DECREASE GFR, MODERATE KIDNEY DAMAGE GFR 30-50% asymptomatic-mild symptoms e.g HT ss mild increase in creatinine, urea anaemia, polyuria, nocturia, hypovolaemia, dehydration 4. SEVERELY REDUCED GFR GFR 10-25%,
51
UTI
inflammation of urinary tract caused by bacteria from gut flora classified according to location predisposing factors age, pregnancy, medical procedures, diabetes, chemotherapy, tumors, antibiotics
52
acute pyelonephritis
upper urinary tract, calyces, medulla usually E. Coli increase neutrophils in tubules usually occurs because of spread from ureter, may also occur due to blood borne diseases can permanently damage tubules- renal damage ss fever, chills, flank pain, proteinuria, pyuria, hematuria, generalised malaise
53
chronic pyelonephritis
chronic renal inflammation severe scarring around calyces, renal pelvis, tubules destruction of tubules, atrophy, dilation, scarring impaired urine conc ability ss dehydration, hyperkalemia, metabolic acidosis, HT, flank pain, dysuria
54
Renal cell carcinoma
malignancy of renal tubular/ductal cells slow growing, can reach a big size before being detected as there is room to grow and the other kidney can function metatisies early to lungs, lymph nodes and bone can grow into vein and renal pelvis ss haematuria, fever, weakness, weight loss, HT, cushing syndrome, hepatic dysfunction, hypercalcaemia, malaise
55
Wilms tumor- nephroblastoma
sporatic genetic mutation,present with enlarged abdomen large mass can occur anywhere in kidney, grow/distort kidney structure ss large abdo mass, HT, pain, vomiting, haematuria
56
Bladder tumors (transitional cell carcinoma)
line the inner surface of bladder, urethra, ureter metastasis via lymphatics to liver, lungs, bone marrow has the tendency to reoccur ss haematuria, dysuria, risk factors men>60, tobacco smokers, industrial exposure to dyes, leather paint, radiotherapy, analgesic use prognosis depends on stage its found
57
mx of renal patients
- if pt meets guidelines for fluid give it to them - morphine is okay in moderate amounts for things such as pain relief - rapid transport ss to watch for - sudden changes in mental status/mood - nausea/vom/ diarrhoea - rapid onset of HT, oedema in feet/hands - rapid onset of numbness,tingling - seizure, muscle twitching - changes in ECG pay close attention to history of illness and timing of physical findings ask about output, and colour